Mönckeberg's medial sclerosis (MMS) is one of the characteristic calcified lesions of uremic artery disease and often exhibits osseous metaplasia. Although its pathogenic mechanism is largely unknown, MMS may contain two different pathologic processes: degenerative process leading to apoptosis or necrosis of medial smooth muscle cells and osteogenic process leading to formation of bone-like structures. It has long been known that calcification follows necrosis. Apoptotic/necrotic cells often release matrix vesicles or membranous cellular degradation products resulting from disintegration of the cells that frequently serve as the nidus of calcification. On the other hand, vascular cells may exhibit osteoblastic phenotype in vitro, and some of the markers for osteoblastic differentiation and noncollagenous proteins regulating mineralization have been demonstrated in calcified arterial lesions. As a possible etiologic factor inducing these two responses, hyperphosphatemia among various metabolic disturbances recognized in uremia may play an important role in the development of MMS in uremia.